Open AccessTargeting Aryl Hydrocarbon Receptor Signaling Enhances Type I Interferon-Independent Resistance to Herpes Simplex Virus
Author(s) -
Jincheng Chen,
Jing Liang,
Hui Xu,
Wenqi Liu,
Shuyan Liu,
Lian Duan,
Fang Li,
Zhaoqin Wang,
Yingxia Liu,
Brian P. McSharry,
Carl G. Feng,
Guoliang Zhang
Publication year - 2021
Publication title -
microbiology spectrum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.502
H-Index - 51
ISSN - 2165-0497
DOI - 10.1128/spectrum.00473-21
Subject(s) - aryl hydrocarbon receptor , herpes simplex virus , viral replication , interferon , biology , virus , receptor , virology , signal transduction , microbiology and biotechnology , transcription factor , genetics , gene
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcript factor that plays an important role in regulating immunity and cell differentiation. However, its role in cell-autonomous antiviral resistance has not been fully elucidated. Here, we show that interruption of AHR signaling in human cells by a chemical antagonist or genetic targeting led to significant reductions in the replication of herpes simplex virus 1 (HSV-1) and cytomegalovirus (CMV), revealing an unexpected proviral function of AHR. Interestingly, the enhanced viral control in the absence of AHR is independent of type I interferon (IFN) signaling. Together, these results reveal a previously unknown function of AHR in promoting viral replication in vitro and suggest a potential intervention point for treating viral disease. IMPORTANCE This study describes how a virus might utilize host aryl hydrocarbon receptor signaling to promote its replication, even in the presence of type I interferons.